Home of the Nouveau-Bese

In and Out —

Teal Deer Warning: The following began as a simple blog post explaining calories in/calories out in response to a number of critics who have challenged my claims that caloric restriction doesn’t work. But once I hit the 5,000 word mark and realized I was drowning these bastards in citations, I realized this would make an excellent chapter for the book I’m writing, which is a detailed indictment of both the $121 billion weight loss industry, as well as the general philosophy that if we just followed Rule X (where Rule X is whatever reasonable method people propose for losing a large amount of weight), we’d all stop being so fat. Unlike yesterday’s Teal Deer, which was more of an exercise in over-analysis, this post actually requires all 10,000 words to dissect this complex and heavily-documented subject. The reason I am publishing this on Fierce, Freethinking Fatties, rather than saving it for the book, is that this information needs to be out there, available, for whoever is trying to explain why dieting doesn’t work. As such, it’s still a work in progress and I’m open to critique and comment, so feel free to throw out whatever questions or comments strike you.

Look up the laws of thermodynamics; they are the laws of the universe as we understand them. The 1st law states that matter and energy can neither be destroyed nor created.

If you worked out your metabolic needs, and ate your daily caloric requirement minus 200 calories, you would absolutely lose weight over time. That’s not an opinion, that is a fact. Leptin and other things can make you want to eat more, but it doesn’t just make fat appear. so, to answer your question: eating less calories than what you burn will result in weight loss, albeit gradual at 200 calories/day.

And if you’re a fat-hating dipshit, then you cite alternative laws (Warning: the second part of the comment at the actual link indulges the hatred of said dipshit, soread at your own risk):

What would happen if you female fatties ate 2000 calories a day? Would your bodies mysteriously defy the laws of physics?

Oh, no, not at all, Dr. AOL, I would never imply that my body defies the mysterious “laws of physics,” including those prescribed elsewhere in the universe. In fact, as Chief Fatty here at Fierce, Freethinking Fatties, I have a strict policy that all of our bloggers must obey every single one of the… what is it, eight, now? Yeah, the eight laws of physics, including, but not limited to, thermodynamics, relativity and quantum mechanics, as well as Newton’s Greatest Hits.

I mean, I’m not a physicologist, but I’m pretty sure that there are some laws of physics that I’ve never even heard of, something like antimatter reduced inversion or something, but we support those laws as well.

Every. Single. One.

And I’d never suggest to Dr. Peter that the research on weight loss failure means that our bodies defy the first law of thermodynamics either. I’ve never proposed that fat people possess cosmic fat glands capable of creating and destroying energy as a mechanism for weight loss resistance. I’ve never said that leptin is the Fat Fairy creating pounds from the tip of her magic spatula wand.

What I am proposing — and what the research has shown for decades — is that the human body has a system in place to compensate for energy expenditure through adaptive thermogenesis. A 2001 study in the British Journal of Nutrition (PDF) describes the effect it has on weight loss:

In summary, these results emphasize the existence of an adaptive component of thermogenesis during weight loss in both men and women, and produced quantitative information on this phenomenon. Moreover, this adaptive thermogenesis seems to be mainly attributable to the energy restriction, since it appeared early in the weight-loss programme, before any major changes in body weight or composition were observed. This finding is reinforced by the observation that once body weight stability and possibly energy balance had been recovered at the end of the programme, adaptive thermogenesis was attenuated, particularly in women where it completely disappeared.

And this is greatest weakness of the calories in/calories out (CI/CO) rule, which claims that with a modest deficit of 200 calories per day through healthy eating and exercise a person will lose about a half pound per week, or around 25 pounds per year, 50 pounds in two years, 125 pounds in five years, and so on. And Dr. Peter’s 200 calorie challenge is modest compared to most mainstream CI/CO deficit of 500 or more calories.

The Mayo Clinic agrees with basic principle of Dr. Peter’s prediction, but prescribes a slightly steeper deficit for achieving a “better BMI”:

Because 3,500 calories equals about 1 pound (0.45 kilogram) of fat, you need to burn 3,500 calories more than you take in to lose 1 pound. So if you cut 500 calories from your typical diet each day, you’d lose about 1 pound a week (500 calories x 7 days = 3,500 calories).

The CDC suggests a 500-1,000 calorie deficit to lose between 1-2 pounds per week (double the caloric deficit, double the pounds lost).

When a company tells you that you can lose 1-2 pounds per week on their program, what is the very next thing you do with that information? Most likely, you’ve calculated how much weight you could lose in a year: between 52 and 104 pounds.

Calories in/calories out, right?

Do I dare oppose the laws of physics and the CDC in single day?

Well, yeah… I guess, since the overwhelming history of research suggests the presence of a homeostatic system that prevents long-term weight loss of greater than 10% for any more than about a third of the population (and that’s an optimistic assessment). If agreeing with that observation means that I directly oppose the law of the universe, the law of the galaxy, then count me guilty as charged.

Because there’s one study that even Dr. Peter suggests as evidence that weight loss is not as straightforward as CI/CO:

The Lancet article you referenced only said that it will take longer for the more obese to reach a steady state and that we need better math models to find basal rates. Ok.

Everyone is born with a basal metabolic rate (BMR), which is how much energy your body spends on a daily basis just keeping you alive (you’re welcome). Because hauling your load around requires quite a bit of energy, your BMR is responsible for 60%-75% of daily energy expenditure, while 10% goes to digestion. Whatever caloric expenditure exercise provides is less than half of our total energy expenditure.

The only thing a person can really do to influence BMR (although it’s not certain how strong of an influence it really has) is to build lean muscle, which is done through strength training. But whether building lean muscle influences BMR doesn’t really matter. Building lean muscle improves insulin sensitivity and does all kinds of other neat stuff.

As far as the influence on BMR, research is mixed, but in a 1990 article in Sports Medicine, researchers found that physically active people could increase their BMR by 5% to 19%. Other studies show no relationship at all.

What research exists does suggest some sort of relationship, although that relationship may be different for lean people and fat people. According to a study in the August 1998 (PDF) Journal of Applied Physiology, 30 physically active, healthy 20-year-olds had a 100 calorie improvement in BMR after ten weeks of resistance training. The average BMR rose from 1,800 to 1,900 calories per day.

But in the September 1997 (PDF) Journal of Applied Physiology, researchers found that after eight weeks in the strength training arm of a randomized trial, 20 obese men and women (ages 19-48) had a decrease in BMR of 125 calories per day. The subjects began the study with the same average BMR as the 30 men in the previous study, dropping from 1,830 to 1,708 calories per day. And in a longitudinal five-month study of strength training in 11 pre-pubertal obese girls, there was no increase in daily caloric expenditure.

I’m pointing this out not to discourage anyone from doing strength training.

Quite the opposite.

I’m pointing this out so people don’t get discouraged that if they’re doing all the “right” things to get healthy, but aren’t having Biggest Loser-style transformations in the first or second or third year (or ever, for that matter), that they shouldn’t feel like a failure and they shouldn’t hate themselves and they shouldn’t stop whatever healthy behaviors they’ve incorporated their lives.

Rewriting the Math

According to the BBC,The Lancet is “one of the world’s most prestigious medical journals,” and the study was led by Dr. Kevin Hall of the National Institutes of Health, along with researchers from the World Health Organization and Columbia University’s School of Public Health. The conclusions Hall et. all draw are remarkably blunt for a paper with these kinds of credentials.

When Dr. Peter says “it will take longer for the more obese to reach a steady state,” this is a breathtaking understatement. The August 2011 Lancet study (PDF) proposes an alternative equation to the CI/CO rule, which the authors refer to as “the myth that a reduction of food intake of 2 MJ per day will lead to a steady rate of weight loss of 0.5 kg per week.” (That’s 477 calories and 1.1 pounds for all you anti-metricationists out there.)

Hall et. al. get straight to the heart of the problem with the CI/CO rule, in contrast to the Mayo Clinic, the CDC and The Big Three (i.e., Weight Watchers, Jenny Craig and Nutrisystem):

This ubiquitous weight-loss rule (also known as the 3500 kcal per pound rule) was derived by estimation of the energy content of weight lost but it ignores dynamic physiological adaptations to altered body weight that lead to changes of both the resting metabolic rate as well as the energy cost of physical activity.

As a person begins eating fewer calories and/or working out, that person’s body composition changes either by reducing fat cells (because you never actually “burn” fat cells, you simply deflate them), gaining (or losing) lean muscle or some combination. As body composition changes, so does the body’s response to caloric deficit and body composition. This response to weight loss is known as adaptive thermogenesis, and it’s the “only” thing standing between you and long-term weight loss success.

And that’s why The Lancet article opposes the idea that the first law of thermodynamics is a formula for weight loss:

Unfortunately, this static weight-loss rule continues to be used for weight-loss counselling and has been misapplied at the population level to predict the effect of policy interventions on obesity prevalence.

We’re a nation awash in obesity policy interventions for an “epidemic” that hasn’t spread since 1999. So, examples of the CI/CO Rule misapplied abound.

Like when researchers predicted that a penny-per-ounce tax would reduce soda consumption by 15%, or a 9 calorie daily deficit, which, using the CI/CO Rule, would mean 867,000 fewer obese fatties over a 10 year period. Based on these estimates, the authors drew some rather optimistic conclusions:

Over the period 2010–20, the tax was estimated to prevent 2.4 million diabetes person-years, 95,000 coronary heart events, 8,000 strokes, and 26,000 premature deaths, while avoiding more than $17 billion in medical costs. In addition to generating approximately $13 billion in annual tax revenue.

If a 9 calorie deficit can have that kind of social impact, then the USDA’s July 2010 research report (PDF) should be an easy sell:

This study estimated that a tax-induced 20-percent price increase on caloric sweetened beverages could cause an average reduction of 37 calories per day, or 3.8 pounds of body weight over a year, for adults and an average of 43 calories per day, or 4.5 pounds over a year, for children.

If a 9 calorie deficit could reduce obese adults by 867,000 and prevent 26,000 premature deaths, then quadrupling that deficit could result in 3.5 million fewer fatties and the prevention of 104,000 premature deaths. Considering obesity is responsible for 112,000 annual deaths, the soda tax alone would cancel out the mortality risk of obesity, right?

This would also bring obesity rates down to the 1970s obesity rates. But comparing the USDA’s CI/CO predictions (known as the static model) with the dynamic model proposed by Hall et. al. makes for quite a gap in expectations.

Despite this gap, the CI/CO rule is so widely accepted that once released, the speculative research on the lives saved became “common sense,” as though they’ve already saved a generation from the grip of obesity. Except we already know that our bodies adapt exceptionally well in order to maintain a stable weight, whether we’re talking about a 9 calorie deficit or 99 calorie deficit. And we know this largely because of the exhaustive amount of research on long-term weight loss.

But considering our national preoccupation with slenderness and weight loss (let alone the $60 billion we spend each year in its pursuit), it’s difficult to believe the commitment to thinness just isn’t there.

But maybe there’s more to the story than simple noncompliance. Perhaps the problem is our reliance on the CI/CO rule.

In an attempt to answer for those dynamic responses to weight loss, Hall et. al. sought an equation that reflected the change in body composition and BMR.

While it is generally recognised that the static weight-loss rule is overly simplistic, there is a dearth of methods for accurate predictions of how changes of diet or physical activity will translate into weight changes over time.

I’ve read a lot of weight loss research for a lot of different methods (e.g., commercial, long-term lifestyle change, low calorie diets, very low calorie diets, low carb, low fat, vegetarian), and reading the Dynamic Rule was the first time I’ve seen something that’s even remotely reflected in the literature.

On the basis of our model, we propose an approximate rule of thumb for an average overweight adult: every change of energy intake of 100 kJ per day will lead to an eventual bodyweight change of about 1 kg (equivalently, 10 kcal per day per pound of weight change) with half of the weight change being achieved in about 1 year and 95% of the weight change in about 3 years. [emphasis mine]

So, while the CI/CO rule says that after one year of a 500 calorie daily deficit you can expect to lose 52 pounds, the Dynamic Model says you can expect to lose 25 pounds after one year and 48 pounds after three years.

Personally, I think that’s still a bit optimistic. That’s why I promote Health at Every Size® (HAES), which takes the emphasis off of weight loss as the primary motivation and benefit. If you think that 500 caloric deficit will result in a 52 pound weight loss after one year, then you’re going to get disheartened rather quickly and, more likely than not, give up eating more fruits and vegetables and exercising.

Unfortunately, we’ve made weight loss the magic prize at the bottom of our barrel of broccoli. When it’s not there we feel conned (because we have been) and we say, “Screw this.” But when we stop making Biggest Loser-style “transformations” seem as simple as calories in/calories out, then people learn to appreciate the true benefits of a healthy, balanced diet and increased physical activity regardless of whether we lose weight at all.

According to graphs A, B, and C, here’s what you get after 6 months, when comparing the Dynamic Model with a randomized controlled trial for three different sets of caloric deficits (PDF): A is a 25% caloric restriction and no additional exercise; B is a 12.5% caloric restriction plus a 12.5% increase in energy expenditure with structured exercise; and C is 890 calories per day until 15% weight reduction, followed by a weight maintenance diet.

Pay particular attention to the black squares (measured bodyweight) and blue line (predicted bodyweight). And for those, like me, who have to look this up every single time, 1 kg equals 2.2 pounds.

Keep in mind, this is merely six months. By one year, the trajectory levels off and by two years the little black boxes are on their way back to baseline. The research is unequivocal in this regard, so researchers are starting to ask the next logical question: is that return to baseline because caloric restriction doesn’t work or because the CI/CO Rule predicting 1-2 pounds per week sets people up for frustration and failure?

Hormones and You

One of the reasons Dr. Peter alluded to for the failure of the CI/CO Rule is that the only way to accurately calculate a person’s BMR is to use a “specialised and expensive doubly-labelled water method.” As it stands, real world weight loss programs have to settle for something like the CI/CO Rule, since estimating the BMRs of people without the expensive test is grossly inaccurate in the best of times:

[U]nfortunately, we cannot measure the initial energy requirements of a free-living individual with a precision better than about 5%… The uncertainty of the baseline energy requirements translates to an expected interindividual variability of weight loss even if adherence to the prescribed diet is perfect. This is a fundamental limitation on our ability to precisely calculate the predicted bodyweight time course of an individual.

Hence, results not typical.

But the bad news isn’t limited to the limitations of our metabolic prognostication. It turns out that how your body responds to caloric deficits depends upon your body composition. The authors give an example of a 100-kg (220-lb) man and an 80-kg (176-lb) man, both of whom are placed on a 2MJ (477 calorie) daily deficit.

There are a few distinct differences in how the two men will lose weight, according to Hall et. al.

First, although the two men may lose the same amount of weight after one year, the 100-kg man will have lost a greater proportion of body fat versus lean muscle. And because the “energetically expensive” lean muscle is preserved, the heavier man can achieve a greater eventual weight loss than the lighter man.

Good news, right?

Then the other shoe drops:

However, to reach half of the maximum weight change takes longer for the 100 kg man than it does for the 80 kg man. Conversely, increased daily energy intake will result in greater weight gain in the 100 kg man than in the 80 kg man and a greater fraction of the weight change will be body fat.

So, the fatter you are, the longer it will take you to reach your goal, and the instant you give up, you regain more fat than the thinner man who does the same thing. And this leads to one of the greatest weight cycling problem: the more you weight cycle, the more lean muscle you lose.

But setting aside the problems of weight cycling, why would the fatter man have a different response to the same caloric deficit? Calories in/calories out, right? Same deficit, same rate of weight loss. Remember 1-2 pounds per week?

[O]utpatient weight-loss interventions typically result in maximum weight loss after 6-8 months followed by gradual weight regain over subsequent years. A common explanation of the weight-loss plateau at 6-8 months is that a metabolic adaptation occurs such that energy expenditure decreases to match energy intake thereby halting further weight loss. Weight regain then occurs as people slowly relax their adherence to the diet that has stopped producing weight loss.

And yet people continue to insist that the issue of weight loss is this simple:

And in popular culture, it sounds something like this:

But we already know this is simplistic bullshit thanks to the work of Dr. Jeffrey Friedman.

Friedman revolutionized our understanding of obesity and health when he discovered leptin in 1994. Leptin is the hormone that affects appetite, satiation and metabolism. Scientists didn’t discover leptin’s partner, ghrelin, until 1996. Ghrelin is the hormone that affects hunger.

So, we’ve only known about leptin since I was a freshman in high school, and they didn’t discover ghrelin until after I finally asked out my first girlfriend and could drive.

This is why I love it when people act like the book on weight loss and obesity has been written (probably by Jenny or Richard or Michael or Gary or whoever spews your particular brand of “truth”), yet we’ve only just begun to understand what the hell’s going on with our weight regulation system.

But here’s what we do know: when you’re hungry, it’s because ghrelin levels have spiked in your body. Then you eat your delicious dinner, and your ghrelin levels gradually fall. As your body’s caloric requirements are met, your body fat creates and releases leptin, which acts as an appetite suppressant.

A more common condition is leptin resistance which, like insulin resistance, is not a problem of production, but a problem of utilization. Fat people tend to have higher circulating leptin levels, suggesting that, for some reason (possibly genetic), heavier people don’t respond to leptin as well as thin people.

A November 2010 study found that patients with higher leptin levels and lower ghrelin levels were more likely to fail at maintaining weight loss at six months. According to lead author Dr. Ana Crujeiras, the influence of hormones may limit weight loss.

“We believe this research is of foremost relevance in clinical terms as it may indicate that the outcome of weight therapy may be pre-conditioned,” said Crujeiras. “Furthermore, our findings may provide endocrinology and nutrition professionals a tool to identify individuals in need of specialized weight-loss programs that first target appetite hormone levels before beginning conventional dietary treatment.”

For the 30 obese subjects who remained on the study for 90 days and who were on doses being studied in Phase 2, the subjects treated with placebo achieved a mean weight loss of 1.5 kilograms [approximately 3 pounds], while those receiving doses that Amgen will take forward to the Phase 2 trials lost a mean of 2 to 4 kilograms [approximately 4 to 9 pounds].

So, until researchers develop a Magic Bullet capable of improving leptin sensitivity, we need to revise the CI/CO diagram slightly:

And until researchers patent a foolproof method for deceiving our bodies with tolerable side effects, I would like to propose that we set aside the CI/CO rule for a more evidence-based maxim: what goes down, must come up.

Fooling Mother Nature

If weight loss were as simple as calories in/calories out, then one would expect to find that the lower the caloric deficit, the greater the weight loss. So, an 800 calorie diet would produce significant weight loss, while a 400 calorie diet would produce even greater weight loss.

Not so, says a November 2001 study in the journal Obesity, in a review of the research on very low calorie diets (VLCDs), which refer to diets between 400 and 800 calories.

A 400-kcal difference in energy deficit per day results in a theoretical total extra negative energy balance of 2800 kcal/week, representing 0.4 kg [0.9 pounds] of adipose tissue. Given the level of accuracy for the body composition methods, differences can only be detected over a relatively long period of time (months). However, both well-controlled RCTs did not show any difference in weight loss over a 6-month period. Also the 1-year results of the Rossner and Flaten study were identical.

A clinically prescribed “healthy” VLCD attempts to reduce the risk of “severe negative nitrogen balance and electrolyte unbalances associated with starvation,” while maintaining dangerously low caloric levels. In theory, a 400 calorie diet should induce a weight loss of one more pound per week than an 800 calorie diet.

The starvation response that supposedly opposes the first law of thermodymics becomes quite noticeable at such a drastic level. But the starvation response is not a trigger that is pulled at a certain caloric level. Adaptive thermogenesis isn’t so much a trigger as it is a rubber band that gets stretched to its limit, then either rebounds or snaps.

The resistance to weight loss, even on VLCDs, is so strong that the average weekly weight loss becomes identical between 400 and 800 calorie diets: around 1.8 pounds.

And for some rather entertaining evidence of adaptive thermogenesis in VLCDs, just peruse the research of commercial weight loss programs to see how difficult it is to spin the terrible long-term adherence, let alone the modest weight loss results. For instance, the Medifast plan prescribes an 800 to 1,000 calorie diet of nutrition supplements, which is less than the very low end of Jenny Craig, Weight Watchers and Nutrisystem, none of which go lower than 1,200 calories.

So, whatever weight loss The Big Three can boast of, surely Medifast has to have superior results.

And indeed, under the before and after photos, Medifast claims that patients can expect to lose between 2 to 5 pounds per week, or 104 to 260 pounds per year, but good luck finding the study that estimate is actually based on.

Medifast’s Research PDF provides the outcomes of nine studies, four of which follow subjects for at least one year. Medifast puts a glossy spin on its research summaries, but the actual results in the research aren’t nearly as impressive as those presented on media resources page (proceed to the end of this blog post to check out the spin provided in each study):

Study 2 — A randomized controlled trial of 119 type 2 diabetics seeking weight loss were assigned to one of two 25% caloric restriction diets, one of which was the Medifast Plus for Diabetics program. Seven subjects dropped out before the start of the program, while just 48 completed the 34-week active weight loss phase. Of the original 54 Medifast subjects, the 31 who remained lost an average of 16 pounds, or half a pound per week. At week 60, 23 Medifast patients lost an average of 11 pounds, or one-fifth of a pound per week. At week 86, 16 Medifast patients lost an average of 12 pounds, or one-tenth of a pound per week. This also means that the average patient who started at 224 pounds spent 86 weeks on the Medifast plan for a final weight of 212 pounds.

Study 3 — An evaluation of Medifast’s medical charts for 1,351 healthy patients (out of 9,948 available records) who were on the Medifast program for at least 12 weeks. Patients averaged between 650-850 calories per day, and some were prescribed 30 mg of Phentermine, an appetite suppressant medication (ASM), for the active weight loss phase. If their hunger persisted, they doubled the dose. If subjects needed a longer-lasting effect, they were prescribed Phendimetrazine. Just 324 (25%) patients lasted 52 weeks, and of those patients, the ones who reported being consistent in using the Medifast supplements and ASMs lost an average of 29 pounds, while those who were not prescribed an ASM lost 30 pounds, or just over half a pound per week.

Study 5 — A randomized controlled trial of 80 overweight kids aged 8 to 15 and 40 parents. After 6 months of a 500 calorie deficit, researchers followed them for an additional 12 months of weight maintenance. No actual weight loss data is provided, and since the study was presented at a conference, only the abstract is available. They do inform us that subjects began the program averaging the 99th percentile. Six months later subjects reached 96.6% and after the full 18 months they were at 96.4%, making the average subject still obese.

Study 9 — A study (PDF) of the effects of a specific obesity gene on the weight loss attempts of 24 obese post-menopausal women. These women completed an average of 13 months on a 1,200 calorie diet, using either a meal replacement supplement or usual care. The meal replacement group either used Medifast or another brand. The study does not indicate how many patients used Medifast, or what the outcomes for those patients were. The only weight loss information provided is stratified by the genetic marker. Patients with the marker lost 36 pounds and those without lost 31.

And there are also two six-month trials:

Study 6 — A six-month open label trial of 47 overweight or obese men and women, half of whom dropped out by six months. Those who remained lost an average 25 pounds, or a pound per week.

Study 8 — An evaluation of a six-month intervention involving 14 low-income pre-bariatric surgery patients on a 1,000-1,200 calorie diet. The 10 who remained after six months lost an average of 27 pounds, slightly above a pound per week.

But when you read the summaries provided by Medifast, you’d think they had finally solved the obesity epidemic. But even with their best spin-masters at the helm, Medifast can’t shake the fact that their long-term results suuuuuuuuuuuuuuuuck.

So how the hell can they claim that “Typical weight loss on the Medifast 5 & 1 Plan is up to 2 to 5 lbs per week”?

One possible source may be Medifast’s 40 week randomized, controlled trial of an 800-1000 calorie diet (PDF). Half of the 90 subjects were assigned to Medifast, and just 28 out of 45 (62%) finished the 16-week active weight loss phase. They lost an average 30 pounds (±13 pounds), or 1.9 pounds per week, give or take 0.8 pounds.

Close enough.

By 40 weeks, subjects in that same study had regained 11 pounds, or a quarter pound per week.

All of these studies raise two important questions: first, why the horrible completion rates? That answer’s simple.

According to Study 3, Medifast patients pay out the nose for the promise of 2 to 5 pounds per week: $150 for initial visit, $75 for one-week follow-up, $65 for monthly visits ($780 per year), and $92.50-$100 per month for supplements ($1,110-$1,200 per year).

If they manage to stick with the program for a full year, that’s an estimated $2,115-$2,205 per year. Let’s be generous and round down. But even at $2,000 a year, patients can expect to lose an average of 30 pounds, which comes out to $67 per pound.

Primal Drives

So, why does this happen? Why, when people achieve a 30-pound weight loss in 16 weeks, do they gain back 11 by 40?

In “The Fat Trap”, a recent New York Times article on weight loss resistance, Tara Parker-Pope perfectly summarizes the long-term hormonal response:

A full year after significant weight loss, these men and women remained in what could be described as a biologically altered state. Their still-plump bodies were acting as if they were starving and were working overtime to regain the pounds they lost. For instance, a gastric hormone called ghrelin, often dubbed the “hunger hormone,” was about 20 percent higher than at the start of the study. Another hormone associated with suppressing hunger, peptide YY, was also abnormally low. Levels of leptin, a hormone that suppresses hunger and increases metabolism, also remained lower than expected. A cocktail of other hormones associated with hunger and metabolism all remained significantly changed compared to pre-dieting levels. It was almost as if weight loss had put their bodies into a unique metabolic state, a sort of post-dieting syndrome that set them apart from people who hadn’t tried to lose weight in the first place.

THIS IS ADAPTIVE THERMOGENESIS

The trick to violating the first law of thermodynamics is that adaptive thermogenesis doesn’t violate the first law of thermodynamics. It simply leverages the first law of thermodynamics to prevent us from starving to death.

But leptin and ghrelin are just the two hormones involved in hunger and satiation. The human body has an array of mechanisms to resist weight loss. A discussion in the 1998 British Journal of Nutrition (PDF) explains the body’s multi-pronged response:

[A] non-specific thermogenesis system reacting to food intake, and three additional systems dependent on ‘memories of body composition’ before weight loss: i.e. a specific thermogenesis dependent on the extent of fat repletion; a hunger-mediated appetite control linked to both repletion of body fat and body lean tissue; and an energy-partitioning system regulating the composition of any body energy change in terms of the relative proportion of protein and fat energy deposited.

The most detailed study of the effects of chronic human energy and protein deficiency was carried out between 1944 and 1946 in an experiment in which 32 healthy young men volunteered to live on the campus of the University of Minnesota while they consumed a diet of approximately 1600 kcal/day, or about two thirds of their normal energy requirement.

In other words, this subjects stayed on the active weight loss phase of Jenny Craig for a full year, rather than transitioning to a higher-calorie “maintenance” phase. Obviously, the effects of long-term caloric deprivation are more severe than short-term caloric deprivation, but the effects of short-term are still striking:

The [resting energy expenditure] of the Minnesota volunteers decreased by 40% after 24 weeks of starvation, thus coming approximately into line with their low energy intake.

After 24 weeks on a 1,600 calorie diet, subjects had balanced their caloric equation through thermogenesis. How does thermogenesis work? First, some energy expenditure will be lost since eating less food means less digestion, which accounts for 10% of energy expenditure. The initial weight loss also means you spend slightly fewer calories on moving around. But something even more fascinating happens to limit our caloric expenditure:

[V]olunteers reduced their voluntary physical activity by more than half, a form of adaptation observed in other studies of chronic starvation and in some, but not all, short-term starvation studies. Nonvolitional or purposeless movements, known as “fidgeting,” can contribute substantially to daily energy expenditure, so reduction in this kind of activity will also conserve energy during prolonged starvation. Such adjustments, when successful, bring starving persons back into energy equilibrium.

This is why you drag ass on caloric deprivation.

“But you should be exercising and eating more fruits and vegetables.”

Yes, I agree, but balancing the caloric expenditure with intake doesn’t necessarily lead to significant weight loss. By now, it should become clear that these systems are called adaptive for a reason.

The more you exercise, the more calories your body craves as fuel for the muscles you’re building. You provide that fuel in the form of calories, whether “good” or “bad.” Eating 5,000 calories of fruit gives you as much energy as eating 5,000 calories of cake.

(Yes, yes low-carbers, I hear your cries and I’ve read Taubes too, but studies of low carb diets don’t have any more impressive long-term clinical (NOTanecdotal) weight loss results than low fat. Low carb vs. high carb is beside the point right now. I’m speaking strictly of the fact that 5,000 calories is 5,000 calories is 5,000 calories in terms of the CI/CO Rule, not whether your hunger is satiated. I’m just pointing out that a larger, physically active person may eat more pieces of fruit per day because they have a greater energy deficit to compensate, but the body’s desire for a certain caloric intake is fairlywelldocumented.)

In the second system, body composition memory, a loss of fat and muscle will trigger leptin and ghrelin levels to compensate and the effects will persist until fat and lean muscle are restored to baseline levels. What’s remarkable about this system is the body’s ability to remember how much fat and muscle you had before the famine began, the level to which your body equates health and stability.

Then, of course, there are the effects of leptin and ghrelin themselves, which influence our response to the food available to us through class and culture.

But most interestingly (to me at least), the body is capable of energy partitioning, which is the body’s way of prioritizing whether we burn the fuel stored in our fat, our liver or our lean muscle. The fact that our body prioritizes energy efficient fat over energy expensive lean muscle shows just how much control our homeostatic systems have over the CI/CO equation.

In a discussion in the 1998 British Journal of Nutrition (PDF), the authors begin by describing the significance of the process:

The regulation of body composition and energy balance is a remarkable phenomenon given that the ability to maintain weight within a few pounds each year with annual intakes of about 4000MJ [955,000 calories] of food energy implies that intake is matched by similar losses of energy to within 1%.

Our three primary sources of energy are stored in distinct organs with protein stored in muscles; carbohydrates circulating freely through the blood blood stream as glucose or stored in the liver or muscle fibers as glycogen; and fat is… well… fat.

Glucose is our primary energy source and is the first type of energy spent. It’s also necessary for brain function. When a person eats carbohydrates and their glucose rises, the body releases insulin which, among other things, triggers the release of an enzyme that transforms glucose into glycogen for backup energy when blood sugar drops.

During a caloric deficit, the dieter consumes fewer energy overall, but when carbohydrate levels drop, so do glycogen stores. Since glycogen is fuel for the brain, the body begins the process of lipolysis, in which the body breaks down the triglycerides stored in our fat cells. The fat cells break into free fatty acids, which fuel the body, and ketone bodies, which may or may not fuel the brain. It’s complicated, so see this footnote**, if you’re a big, fat nerd.

Low-carb dieters deprive the body of carbohydrates/glucose, which triggers ketosis, the state of elevated ketones in the body. An excess of ketones in the body can lead to ketoacidosis, which increases the acidity of your blood. In diabetics, ketoacidosis can be fatal. Low-carb diets done with physician supervision won’t typically lead to ketoacidosis, but low-carb diets do make mild ketosis a way of life.***

According to the Mayo Clinic, if you’re diabetic and exhibit any of these symptoms, it could be ketoacidosis and you should seek medical assistance immediately:

Excessive thirst

Frequent urination

Nausea and vomiting

Abdominal pain

Loss of appetite

Weakness or fatigue

Shortness of breath

Fruity-scented breath

Confusion

But according to my friend Laurie, the nurse practitioner, diabetes educator, and all-around badass, the only symptoms that are specific to ketoacidosis are nausea, abdominal pain, confusion, coma, and heavy-labored fruity-smelling breath (called Kussmaul respirations). The others are symptoms of low blood sugar

The most frequent complaints with low-carb diets are constipation and headache, which are readily explained by the lack of fruit, vegetables and whole grains, Astrup said.

Also, bad breath, muscle cramps, diarrhea, general weakness and rashes are more often reported on low-carb diets than on low-fat diets, Astrup found.

The body becomes so desperate for the glucose energy of carbohydrates that when the low-carber inevitably “falls off the wagon,”**** the body simultaneously stores as much glycogen and free fatty acids as possible. Triglycerides store twice as much energy as glucose or protein, which is why the body wants to replete fat stores after the famine. It is only because of our dynamic fat stores that our ancestors were capable of surviving a famine at all.

But should the dieter persist and deplete both glycogen and fat storage, the body must finally dip into its emergency fund: protein. Protein catabolism breaks down the protein stored in muscles into amino acids and derivatives.

The catabolic state can be caused by a prolonged stress response or nutritional deficiencies. The long-term result of protein catabolism is the loss of lean muscle, including the heart. Even without the cardiac damage, it’s foolish to waste lean muscle, since it requires more caloric energy, which burns off the excess glucose that triggers insulin resistance. Forget thinness, the goal of exercising and building muscle is to burn off excess glucose and reduce the strain that excess insulin puts on your system.

The Ancel Keys’ Starvation Study***** found that subjects lost a significant amount of lean muscle, comprising the majority of weight loss on the 1,600 calorie diet:

The Minnesota volunteers lost an average of 23% of their initial body weight and more than 70% of their body fat. Muscle was also lost: in all, 24% of the lean tissue mass (termed “active tissue mass” in the study) was lost, and this accounted for 60% of the total weight loss.

Bear in mind that a 23% initial weight loss is still less than the weight loss ideal of women according to a 2005 randomized trial (PDF) in the International Journal of Obesity:

Many obesity treatment programs recommend weight loss goals of 5–10% of body weight, in the belief that such goals are achievable and clinically valuable. Program participants typically select much higher goals, however.

The trial included a self-reported survey and followed 1,801 health plan members for two years. At the beginning of the study, the authors asked basic health questions and, in addition, two questions on their weight loss goals:

Weight goals were calculated in two ways: goal weight loss from ‘How many pounds do you expect to lose in the Weigh-to-Be program?’ and ideal weight loss from ‘How much would you like to weigh?’

Women had a 21% weight loss goal and a 27% ideal weight, while men had a 16% weight loss goal and 19% ideal weight.

So it works, but only by starving yourself for a prolonged period of time and wasting a quarter of your muscle mass just to achieve an arbitrary weight goal. Fortunately, it’s extremely difficult to intentionally starve yourself, unless you trigger an eating disorder like anorexia, the deadliest mental illness.

For the vast majority of the population, however, when we reduce our energy intake, our body prioritizes energy expenditure in a way that protects our body weight while doing the least amount of damage to our bodies for as long as possible. However, the longer you successfully maintain that caloric deficit, the more damage you will ultimately do to your body.

Rounding Up

What would happen if I cut back my caloric consumption by just 200 calories? Well, the CI/CO Rule says that a person might lose a pound every 2.5 weeks, or 21 pounds after a year. But Dr. Peter defends the Adaptive Rule’s rate of weight loss as “gradual”:

However, according to Adaptive Rule, a 200 calorie deficit would lead to a 10 pound weight loss after one year and 19 pounds after three years. Now that’s gradual.

Whether you choose the “gradual” approach or the VLCD extreme, the disappointing results typically come down to the foods that are available to us, according to the pithy summary in a 2004 report in the Journal of the American Dietetic Association.

To create and consume a satisfying diet with high intrameal and intermeal satiety, we ideally want our diet to consist of low-energy-density foods with high palatability; however, such foods do not commonly exist… Unfortunately, foods that are low in fat and energy density, especially the more palatable of these, are typically more costly and/or inconvenient to purchase or prepare.

And that is the fourth nail in the coffin of the CI/CO rule. Between adaptive thermogenesis; the ridiculous expectations for weight loss; the difficulty and expense of living on a low-energy-density, high palatability diet; and the infinite combinations of stress and disruption in the average year, you’ve got a recipe for embarrassing drop-out rates and modest long-term weight loss for every single weight loss program and philosophy.

Every. Single. One.

What I’m proposing isn’t new and it isn’t a surprise to anyone except those who aren’t familiar with the research. When you listen to the real experts, the ones involved in the research of obesity, weight loss and nutrition health, you find that what I’ve outlined above is well-established and accepted by the medical and research community, but few people actually say it publicly, or if they do they issue enough caveats to nullify the original truth.

A great example of someone publicly speaking truth on the subject of weight loss comes from a 2006 episode of NOVA featuring Dr. Michael Rosenbaum of Columbia University, who worked on low-dose leptin treatments to aid weight maintenance, as opposed to the failed high-dose weight loss treatments:

Well, when you try to maintain a reduced body weight, your body fights back. So, for example, if you were to lose 10 percent of your weight—and it doesn’t matter if you’re fat or thin, a couch potato or a trained athlete — the number of calories you’ll require to maintain that reduced weight will fall by over 20 percent. That means that if you lose 10 percent of your weight to, say, about 150 pounds, you are going to require about 300 to 400 calories a day less to stay at that weight than someone who naturally weighs 150 pounds. Alternatively, you will have to increase the number of calories you spend exercising by 300 to 400 a day to stay at that weight.

Jason Alexander didn’t set his sights on extreme weight loss—and that may be his secret to success. The pleasantly plump actor turned to Jenny Craig to lose just 30 pounds. By slashing his daily caloric intake from 4,500 to 1,500 and adding regular workouts, he was able to drop the weight in 6 months.

A 3,000-calorie deficit and increased exercise would mean 21,000-calorie weekly deficit and, according to the CI/CO Rule, Jason Alexander should have lost 6 pounds per week, or 144 pounds after 24 weeks (6 months).

First, he doesn’t have 144 pounds to lose, but more importantly, in order to lose just 30 pounds in six months he had to eat 1/3 of his caloric intake and exercise regularly for a before and after picture that looks almost identical. As Shape points out, he didn’t even set his sights on extreme weight loss. This is what he had to do for modest weight loss.

So, Dr. Peter, and anyone else who continues to believe that weight loss is as easy as calories in/calories out, you can continue to deny that our body fights caloric deprivation, but my claims are made from the shoulders of giants in the field of obesity research. And considering Friedman’s contribution to our understanding of the process, I’m betting there will be decades of fascinating research pulling apart this system.

I’m not too concerned as to whether learning about adaptive thermogenesis will lead to effective weight loss treatments.

The evidence already shows how much healthier we can be when we stop emphasizing weight loss for fatties and start emphasizing healthy options for all.

Afterword

*Okay, so there are 1, 2, 3, 4, 5, 6, 7 studies that support the idea that ketones are fuel for the brain, but Laurie says otherwise:

I am not sure where this comes from, but I have always been told that the brain can only use sugar for fuel. If the blood sugar drops you immediately have severe effects on the brain and will lead to coma and death. Why can’t they use ketones for fuel when their blood sugar drops? If the brain could use ketones for fuel, why do they go into a coma when they are in ketoacidosis? I think people just get confused. When they are in starvation ketones go up because they are burning fat for fuel and ketones are a byproduct of the fat burn. The reason they do not get severe elevations in ketone when on a starvation diet is that they can also use protein for fuel which decreased the speed at which they are burning fat, giving the kidneys time to get rid if the ketones.

I have since asked multiple friends in the medical field whether ketones can be burned by the brain for fuel. Their initial response is no, but when I present the low-carb case, they tend to hedge. So, there is something to the claim that traditional medicine isn’t teaching the ketones-as-fuel theory. However, there is still the question of whether ketones are an optimal fuel. For example, protein can be used as a fuel source for the body, but its by-product is blood urea nitrogen (BUN) and contemporary medical opinion is that an excess of BUN is toxic for the body. So, it’s an extremely complicated and controversial subject, which I will set aside for now for simplicity’s sake.

****In a July 2004 article in Cardiology recommending that the low-carb lifestyle be taken seriously, Dr. Joel Gore substantiates his case with retention rates of 76% in one 24-week study and 69% in a one-year study. And after a two-year randomized trial, the authors found slightly lower retention rates for participation in the study (although it does not account for whether a person is still adhering to the low-carb diet). And adding insult to injury, low-carbers had higher drop-out rates:

In the low-fat group, 6%, 12%, 25%, and 32% of participants did not participate in assessments at 3, 6, 12, and 24 months, respectively. Values for the low-carbohydrate participants were 9%, 16%, 26%, and 42%, respectively.

This means that of the 153 people who participated in the study, 89 showed up for the final assessment two years later. What percentage of that remained still followed the low carb lifestyle is anyone’s guess. I’m guessing low adherence is how low carbers would have to justify the awesomeness that is the two-year results for low-carb vs. low-fat:

The only thing a low-carber can boast about here is that HDL is slightly higher for it than the low-fat group, as the paper summarazies:

We found a significantly greater decrease in LDL cholesterol levels at 3 and 6 months in the low-fat group than in the low-carbohydrate group, but this difference did not persist at 12 or 24 months. Decreases in triglyceride levels were greater in the low-carbohydrate than in the low-fat group at 3 and 6 months but not at 12 or 24 months. Decreases in VLDL cholesterol levels were significantly greater in the low-carbohydrate than in the low-fat group at 3, 6, and 12 months but not at 24 months. Increases in HDL cholesterol levels were significantly greater in the low-carbohydrate than in the low-fat group at 3, 6, 12 and 24 months. The ratio of total cholesterol to HDL cholesterol levels decreased significantly in both groups through 24 months but did not significantly differ between groups at any time. There was a trend for greater reductions in the low carbohydrate group at 6 months (P 0.035) and 12 months (P 0.016) (Table 2). Therefore, the only effect on plasma lipid concentrations that persisted at 2 years was the significantly greater increases in HDL cholesterol levels among low-carbohydrate participants.

And in terms of weight loss, both low-carb and low-fat do the double-digit dip, with low-carb dropping slightly more and bouncing back slightly more as well.

Sorry, low-carbers, but your lifestyle’s failure looks just like low-fat to me. Likewise, the handful of long-term success stories, who are then eligible to be classified “expert” on the subject, are just as unimpressive to me.

*****I know, I know, low-carbers, you’re just itching to tell me all about how Ancel Keys is a douchebag who fucks a loaf of bread every night. I understand, but please try to understand that this post isn’t about you. I’m sure I’ve got some other low-carb post you can search for. But if you want to ask a question, I’ll most likely save my response for a future post because it’s such a complicated subject and our comment threads don’t lend well to that.

Study 2 Spin: “Our main study finding was significantly improved weight loss over 8.5 months (34 weeks) among those randomized to meal replacements compared with a standard, self-selected, food-based diet. Among completers, participants in the PCD group were 5 times more likely to lose 5% and 6.5 times more likely to lose 10% of their initial body weight at the end of the active weight loss phase than were participants in the SD group.”

Study 3 Spin: “The results of combining both obesity pharmacotherapy and MMRS produced substantial and sustained weight losses that were superior to those typically reported in drug and meal replacement studies, particularly those lasting at least one year. Thus, the combining of obesity pharmacotherapy and MMRS appears to substantially enhance weight loss beyond that typically produced by either alone. In addition, our completers’ data demonstrated that the majority of patients reporting using the medications and MMRS fairly consistently experienced the best average weight losses (although the difference was not stastically different from those who were less consistent).”

Study 5 Spin: “Among overweight 8–15yo children, dieting with or without a parent, meal replacements were as safe and effective as a food-based diet for weight loss and maintenance.”

The best research results come from very low calorie diets (VLCD), defined as a daily intake of 600-800 calories. VLCDs are only available to those with a BMI over 30, or a BMI over 27 with complications. While weight loss on VLCDs average slightly higher and last slightly longer than higher-calorie prescriptions, long-term results are still disappointing for the vast majority.

In the February 1999American Journal of Medicine, a one-year study compared VLCDs with and without sibutramine, the generic form of Meridia, an appetite suppressant which Abbott Pharmaceuticals pulled off the market in 2010. According to Bloomberg, “16 percent more major cardiovascular side effects in a study of 10,000 high-risk patients who were followed for as long as six years. An estimated 100,000 Americans now take Meridia and Abbott no longer promotes the drug in the U.S.”

But authors of the study were pretty optimistic about its effects:

Following a very-low-calorie diet, sibutramine is effective in maintaining and improving weight loss for up to 1 year.

How effective? Well, after one year, the 81 patients with sibutramine lost an average of 12 pounds (±17 pounds), while the 78 on the placebo lost 1 pounds (±13 pounds).

Impressive.

In the 1989 International Journal of Obesity, Stunkard et. al. published the results of a five-year VLCD clinical trial with 76 obese women. Participants had average age of 42 and weight of 233 pounds. Subjects were randomly assigned to either VLCD alone, behavior therapy alone or a combination of VLCD and behavior therapy.

At the end of treatment, the VLCD and therapy groups lost an average of 29 pounds, while the combined groups lost 37 pounds. One year after treatment, the VLCD, therapy and combined groups maintained an average weight loss of 10, 15, and 23 pounds, respectively. And here’s the kicker: while one-third of the therapy and combined treatment subjects maintained their full end-of-treatment weight loss after one year, just 5% of VLCD subjects did so.

Therefore, if, for some reason you’re bound and determined to lose weight, then you’re looking at an average of 23 pounds after one year of starvation and therapy. As if that weren’t motivation enough, Stunkard concludes starkly:

Five years after treatment, a majority of subjects in all three conditions had returned to their pretreatment weight, and 55 percent of the total sample had received additional weight reduction therapy.

Not all researchers feel the news on VLCDs is all bad. In fact, Wim Saris published a rather friendly review of the VLCD research in the November 2001 journal Obesity Research. Saris wrote a rather sanguine conclusion for the abstract, “VLCD with active follow-up treatment seems to be one of the better treatment modalities related to long-term weight-maintenance success.”

He goes on to outline the history of VLCDs, beginning with the research of Evans and Strang in 1929, and going through the popularity of VLCDs in the diet-mania 70s:

In the 1970s, this dietary weight-loss concept was reintroduced with great success by Blackburn et al. and Mclean Baird et al. These studies attracted commercial interest, especially in the United States. Unfortunately the commercial use of hydrolyzed collagen as the only protein source and no inclusion of adequate amounts of vitamins, minerals, and electrolytes in a “liquid-protein diet” seemed to be fatal as reported by the U.S. government

Modern VLCDs are more nutritionally balanced now, so VLCDs are safe Saris assures us. Besides, they’ve never actually proven that VLCDs killed anyone:

Although extensive research never revealed a direct link between the reported deaths and the use of this liquid-protein diet, the adverse publicity has marked VLCDs for many years. Nevertheless because of the success of a number of nutritionally complete commercial VLCDs, several million people have used VLCDs and lost tons of weight as calculated for the United Kingdom, without reported deaths. Also because of the efficacy of the method to lose weight, VLCD is by far the most extensively used weight-loss method in the scientific literature.

Of course, whatever “success” we’re led to expect comes with a serious caveat:

There are a number of minor but bothersome side effects of VLCDs. Most cited are the following: dry mouth, constipation, headache, dizziness/orthostatic hypotension, fatigue, cold intolerance, dry skin, menstrual irregularities and hair loss. Most of these effects are directly related to the negative energy balance situation.

Coincidentally (or not), according to the Mayo Clinic the “minor but bothersome” side effects of anorexia nervosa include dry skin, frequently being cold, menstrual irregularities, dehydration, constipation, low blood pressure. And the “minor but bothersome” side effects of low blood pressure include fatigue, thirst, dizziness, cold, clammy, pale skin, and fainting.

Saris goes on to confront what he perceives as a common misconception:

Both among laymen and professionals it is believed that the initial greater weight losses achieved with VLCD is followed by larger weight regains ending in an even worse body-weight status. These ideas are partly based on the observation that, with a more profound energy restriction, adaptive mechanisms to preserve energy occur, such as the decline in resting metabolic rates. Therefore, the general advice is to achieve weight loss at a slow rate in order to preserve it.

In response to the adaptive mechanism, Saris cites two studies:

A 1997 randomized comparison in the British Medical Journal followed 43 obese adults who were placed on either 8 weeks of a 420 calorie VLCD or 17 weeks of a 1,250 calorie conventional diet (CD). Both groups had a weight loss goal of 30 pounds. Subjects on the VLCD lost 3.5 pounds per week while subjects on the CD lost 1.5 pounds per week. Patients were also given an appetite suppressant compound comprised of three daily doses of ephedrine (20 mg) and caffeine (200 mg). After their respective active weight loss periods, both groups lost an average of 28 pounds. Following the active weight loss phase, subjects were randomized into one of two groups: “one year weight maintenance programme of ad lib, low fat, high carbohydrate diet or fixed energy intake diet (≤7.8 MJ/day [1,820 calories/day]), both with reinforcement sessions 2-3 times monthly.” After one year on the weight maintenance programs, the fixed energy and ad lib groups had maintained a weight loss of 30 pounds and 21 pounds, respectively. But just one year after the maintenance phase ended, the fixed energy group had regained 25 pounds, while the ad lib group regained 12 pounds. Saris’ conclusion: “Although the differences did not reach statistical significance, the outcome of this study with this special design at least does not support the idea that rapid weight loss negatively affects long-term success.”

A 1997 randomized controlled trial in the Archives of Internal Medicine followed 59 morbidly obese adults with a mean weight 293 pounds. Subjects were either assigned to behavior therapy (BT) and a VLCD or BT alone. After the eight week active weight loss phase, the combined group lost 50 pounds, while the BT only group lost just 20 pounds. Unfortunately, just 44% of the combined subjects remained at the end of the eight week weight loss phase, while just 28% of BT subjects dropped out. After five years, the combined group maintained a loss of 37 pounds and the BT only group maintained 11 pounds. Saris’ conclusion: “The study by Pekkarinen and Mustajoki, with an 8.9 kg and 22.2 kg initial weight loss, shows much better long-term results after 5 years.”

Interestingly, there’s also a chart comparing the long-term weight regain from nine randomized controlled trials which Saris says “do not indicate such an adverse effect.”

Like this:

Related

If decreasing your caloric intake by 200 calories per day would result in a 104 pound weight loss in 1-2 years…then a 5’2″ 104 pound woman who decreases her caloric intake by 200 calories per day would disappear entirely in 1-2 years…. wrong…how do you explain that, Dr. Peter? Miraculous? I can’t believe it’s not obvious to everyone that nothing is that simple.

*I’m reading this opus in parts, so I apologize if I’m duplicating something here.

OK guys, (y’all). It is all in my book. Fatology 101. I just feel that there are thousands of diet books out there and now it is time for us. We need to get thousands of our books out there. Ragen, Loni, and I all have books that talk about the “bull shit” that is out there and all the misinformation. Like I have said before, I am all about telling the world we are born fat, get over it. It is not about food. Never has been. Until we can get the message out there and the world can see our message, it will always be that obesity is about the calories in/calories out MYTH!!! Good luck with your book. We will get it done.

Wow, that’s a lot of research you’ve done there! Hope you enjoyed doing it. Anyway, this is based on my own experience is that if you weight cycle you don’t lose heaps of muscle. I’ve yo-yoed 150kg over the last 20 years (in bits an pieces – not all at once) and really I haven’t noticed any change in the amount of muscle on my body. So by that, if you yo-yo once you lose a certain amount of muscle. If you yo-yo 5 times you might lose a bit more. But if you yo-yo 100 times (admittedly it’d take you a century or two) I doubt the amount you’d lose would be more than the amount you’d lose after 5 yo-yos.

Also I’m sure that as you gain fat, you also gain muscle since your body needs to move more body around. As you lose weight, you don’t need so much muscle to move around, hence you lose some muscle.

John,
While I understand what you’re saying, you can’t use anecdotes to counter research, especially in this case. You’re basing your assumptions on how your body feels, not what its actual composition is. The only way you can know whether you’ve lost muscle is by using a DEXA scan, which measures actual body composition. The studies I cite base their estimates of muscle loss on DEXA scans.

Also, even if you lose weight, you can rebuild some muscle through strength training. It’s not that it won’t come back, it’s that when people lose, then regain, they typically regain more fat than muscle. So, with each cycle you lose a little muscle, gain a little fat. And if you’re building muscle, you won’t be losing weight, since muscle is denser than fat. Also, I have not read any studies on whether muscle loss is affected by the law of diminishing returns, but I don’t think you can simply guess at it and assume that’s correct.

Last fall I went to a bariatric doctor to help me lose weight (an anti-WLS doc). His program was all about low-carb and low-calorie diet with a first phase and then a second “maintenance” phase.

I was restricted to a max of 75g of carbs a day (none at breakfast) and 1,200 calories per day. I lasted….5 months?….until gradually falling off the wagon. Which, to me, is a marathon of a damn diet like that. I did lose about 30 pounds, and it was all without exercise. Reeeeal healthy, right? Ugh. I wonder how much more I messed up my body by participating in that (because I’m sure it was already pretty damn messed up before with a lifetime of on-and-off diets!).

Needless to say, I was absolutely miserable on that diet. Which is a big reason why I didn’t exercise in the slightest. I was too depressed to do anything but sit on the couch and daydream about food.

And that diet still lingers with me. I wish I could shake it off–I wish I had never gone on it at all. I’m continually struggling to not regain my weight (floundering between 5 & 10 pounds regained at this point) and it’s not a great way to live. It’s left me worse off with disordered eating than I ever have been and I don’t think those 30 pounds were worth it (I still had 40 pounds to go to reach MY goal weight).

I just realized the day before yesterday (when I took a gander at a BMI chart), that when my doctor asked for my goal weight I said 135. It was just a number I pulled out of thin air that I thought would get me a good weight where I would be happy–I had no clue where it was on the BMI scale, but I was sure it wasn’t “too skinny” for my 5’1″ height. His response? He wanted it to be lower than that–I think 125? Possibly even less, but I don’t remember. Then the other day I realized that my 135 goal was smack dab in the middle of “healthy” weight, whereas 125 would probably put me at “underweight” or at least bordering that. Jackass.

Thanks for the research! I should send this to my brother–he’s a firm believer in the CI/CO myth.

You’re welcome Rapunzel, and sticking with a 1,200 calorie diet for 5 months is impressive in terms of self-restraint. The Minnesota Starvation Experiment had subjects at a 1,570 calorie level and they had to be monitored constantly because some were compulsively cheating (a side effect of semi-starvation).

Also, your inactivity during this time is also due to the leptin/ghrelin influence. There are studies that show that when you reduce your caloric intake, your body responds by influencing your caloric expenditure. So, mice that are restricted will suddenly become lethargic. It makes sense… no energy, no movement. And the psychological effects of starvation are also well-documented. Suffering depression is no surprise at all. There’s research that ties low leptin levels to increased depression.

This is why leptin is my favorite hormone… its effect on the body is so wide-spread and so diverse that it’s kind of mind-boggling. And when we tell people that caloric restriction is the key to being healthy, we’re ignoring the subsequent health effects that chronic low-leptin levels have on both physical and mental health.

I wish you the best on your path to health and that you might shake the residual effects of that diet. Good luck!

Yeah, the health outcomes seen populations of people in the BMI overweight category aren’t particularly anything to write home about. Generally doctors get pushy at that level of weight because they hope to stop someone from moving into (or back into) the obese category, where negative outcomes are more highly associated. From a relative risk position only, having a BMI from 25-29.9 isn’t particularly any more risky than having a BMI of 24.9 or lower, but having an “overweight” category BMI puts one at higher risk for moving into the “obese” cateogry of BMI which has the higher risk. Especially since it’s generally expected as one ages they will put on some weight. If that makes sense.

This may be true for populations, but it doesn’t make sense to apply it to individuals. Different weights suit us (at the same height) at different times in our lives and 125 might very well be suboptimal for Rapunzel. The so-called “overweight” range is actually at least as healthy as the “normal” one when considering populations.

Calories in vs. calories out isn’t “bullshit.” It’s completely true, but despite being simple at a macro level, it’s very complex at a micro level, such that someone could write a whole lot of words about all of the mechanisms involved in the system; and yet, all of that has little impact on the practical side of weight loss.

It is bulls*&%! So how does one measure the calories out? Has anyone measured the poop that is going out? That has a lot of calories in it. Do the math. Eat 1000 cal. in a day, the body uses some, lets say on the low side, 700 calories, and the poop has about 500 calories….ooops doesnt add up. Yes, I am just throwing out numbers…sounds like all the diet gurus out there just throwing out numbers. There is no proven way to count the calories one uses. There are too many variables, hormones, heat loss, POOP! Come on use your common sense Steve.

“Has anyone measured the poop that is going out? That has a lot of calories in it.”

Yes, notably Wilbur Atwater, who developed the Atwater factors, which are the numbers which appear on modern nutrition labels. Healthy people don’t excrete many calories; the digestive system is quite efficient. However, there is already a correction for excreted energy built into nutrition labeling. Although those corrections are sometimes based on averages and so may be off one way or another for any given food item, excreted energy is not likely to be a large source of error in calorie counting.

There are ways to burn calories and ways to conserve them; many of these are out of our conscious control. Usually, the body sticks to a weight range and adjusts its conserving and burning mechanisms to keep you in or cose to this range, which varies from person to person.

No one has the ablility to measure calories in and calories with the amount of variables involved. Lets take a few examples. The freshman 15 is a good one. If you do the math, a college aged person will gain 15 lbs in 4 years. That is only 47 calories a day. Doesnt make sense. Also, there are fat cells. If, for the sake of explaining, one person has 1m fat cells and another has 2m. Who is fatter? Depends, if the size of the 1m is the size of a quarter and the 2m is the size of an asprin, then the person with 1m would be fatter. You dont have control of the amount of your fat cells or how many your body produces. Please take a look at my book Fatology 101. You can read some of it on Amazon if you dont want to buy it. With all humility that I can write, people are born fat, thin, tall short etc. Just let people live. Thank you

And the sun rises in the east and sets in the west. No wait, the earth is actually rotating around the sun. OOOPs.Trees grow to 10 feet and some grow to 12 ft. Come on everything in nature is different. No 2 of anything are the same except twins. How come we are born, tall, short, blue eyes, brown eyes, big feet, little feet, thin…..on and on yet no one is born fat!!!! We are different and calories have nothing to do with it. I cant change your mind, any more than changing the minds of those who believe the world was flat. If you are not willing to check it out for yourself and learn that things arent always as they seem because someone said so without any evidence then there is nothing more to say.

You really have to ask that question? With people dying of starvation all over the world, you really have to ask that question? I can show you people who have had WLS and died because they starved to death – their digestive systems were so mutilated that they could no longer absorb the nutrients from what little food they could eat, even though they were also taking supplements. When one takes in less calories than their body needs to survive, and does this on a daily basis for weeks/months/years, their body starts to cannibalize itself in order to try to survive (and all that does is hasten its demise). Don’t bother us with your specious questions about how does anyone starve to death. You know perfectly well it’s possible, it happens every fucking day somewhere on this earth.

The human metabolism (and I’d argue the metabolism of any living thing) is absolutely adaptive Jacques. The body easily adjusts to smaller changes in caloric intake. But when you take that to an extreme the body tries and fails to regulate, there’s only so much to turn down or off until you start to get catastrophic failures that result in death. A great example would be menopause in anorexic women. Farther down the spectrum, people who are starving get increasingly more sluggish and ill until their systems become so compromised that they succumb either to organ failure or to some bug their immune system could no longer fight off.

That’s a pretty silly question, I doubt there’s any one single answer to that question. It could be anything from age, gender, personal characteristics, previous diet, body fat, muscle mass, bone density, immunity, location.

Of course, why didnt all the starving people in WW11 prison camps die? They are all different and process calories differently. Why today do some people gain and some lose eating the same things. This is where the whole problem begins. Being fat isnt about food. It is how each body responds differently to food as well as anything else, meds, etc.

I’m not sure why you’re so invested in the net caloric balance thing. Yes, in the absence of no food, someone will lose weight and then die. They may very well die well before they lose all of their fat, because using up one’s own bodily resources isn’t sufficient to maintain health and starvation puts stress on the system.

My point is, what does the net caloric balance thing matter? There are some, if not many people, who can not reduce their caloric intake past the point where their body can easily adapt to the change intake (and maintain excess fat) in and still be functional for every day life. So what does it matter, if such caloric intake has no real world effectiveness, even if it would have at least short-term *efficacy* if you locked someone in a lab for several years. It’s not practical and it has no bearing in a conversation about real world weight loss and weight maintenance.

In science, BOTH theroies AND laws can be shown to be wrong at some time if there are data to suggest it. There is NO HEIRARCHY WHATSOEVER between theories and laws. In science, laws CAN BE CHANGED JUST AS EASILY as theories. A law could change TODAY if there is new evidence.

In science, laws are NOT immutable. That is not even a property of a law , you uneducted Internet fool.

Furthermore, you are MISUSING thermodynamics to SOUND scientific and BLAME obese people.

Science does not at all understand the chemical behavior of fat cell receptors.

Mice became OBESE WITHOUT consuming more claories. Thee are at last 4 ther studies shwoing this same type of thing.

Every law and theory in science has a SCOPE OF APPLICABLITY, you uneducted fool.It is VERY COMMON in science for laws to ONLY apply under certain circumstances and not others.

The JOB of physicists is to find the results in which our current understanding of physics is WEONG. From there NEWER, “less wrong” or “more correct” theories devlop. That is how science works, you ignorant anus.

YOu are just a diet industry SHYSTER MISUSING thermodynamics in an attempt to oversmplify an extremely complex BIOLOGICAL PHENOMENON CALLED OBESITY.